Increased Dickkopf-1 expression is correlated with poisoning severity in carbon monoxide-poisoned humans and rats.

CONTEXT:Carbon monoxide (CO) poisoning results in neuronal injury. The expression of Dickkopf-1 (DKK-1) has not been investigated previously after CO poisoning. OBJECTIVE:The current study aimed to investigate the DKK-1 expression levels in humans and rats with acute CO poisoning and to analyze their correlation with poisoning severity. MATERIALS AND METHODS:We measured serum DKK-1 levels in patients with acute CO poisoning (n = 94) and in healthy controls (n = 90). On admission, a poisoning severity score (PSS) was determined for each patient. In addition, 36 male Sprague-Dawley rats were randomly assigned into three groups: (a) Sham group, (b) Low CO group and (c) High CO group. At 2 h after CO poisoning, DKK-1 expression and histopathological damage in the hippocampal tissues were measured. RESULTS:Serum DKK-1 levels were significantly higher in the acute CO-poisoned patients, compared to the healthy controls. Serum DKK-1 levels were significantly higher in the CO-poisoned patients with a lower PSS. In rats, CO poisoning induced significant upregulation of the gene and protein expression of DKK-1 in hippocampal tissues. Moreover, there was a positive correlation between DKK-1 levels and the degree of damage in the hippocampal tissues. DISCUSSION:DKK-1 induction in neurons after CO poisoning causes further neuronal injury. The severity of acute CO poisoning in rat models is associated with elevated serum DKK-1 levels and its upregulation in the brain tissue. CONCLUSION:DKK-1 appears to have potential utility in providing valuable information for determining the severity and damage of CO poisoning.

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